Biomedical subjects

J Kåhrström

Publications and source records attributed to J Kåhrström.

At least 19 recordsLinked to original sources

PubMed1996

Neonatal pre-ganglionic sympathectomy affects morphometrically defined architecture in rat cerebral arteries.

In order to clarify further the nature of the long-term influence on the cerebral vasculature by the sympathetic nerves, a bilateral cervical pre-ganglionic denervation was performed in 1-week-old rats. Four weeks later, morphometric determinations of the vascular dimensions revealed diminished media cross-sectional areas and luminal radii in the middle cerebral and posterior cerebral arteries, whereas these parameters were unaffected in the basilar artery. In the latter artery, however, a 40% increase in the cross-sectional area of the internal elastic membrane was found. No re-innervation of the denervated ganglia occurred during the course of the experiment. The results suggest that the long-term effect exerted by the sympathetic nerves is associated with the nerve activity, rather than being a true trophic influence.

Animals↗

PubMed1996

Neonatal chronic sympathectomy in normotensive rats affects pial arteries: enhanced stiffness and reduced capacity to dilate.

The functional implication of previously shown effects on pial wall morphology by sympathectomy was tested. Following either ganglionic or pre-ganglionic denervation in 1-week-old rats the passive arterial compliance was reduced in basal cerebral arteries of 20-week-old normotensive, but not of hypertensive animals. The magnitude of the denervation induced stiffness was similar to the alteration seen in spontaneously hypertensive rats when compared with normotensive animals. No difference was seen between the two types of denervation. Following ganglionic sympathectomy in 1-week old normotensive rats-and examined 19 weeks later-the increase in cerebral blood flow (measured with the [14C]butanol sampling technique) induced by high arterial CO2 concentration was attenuated compared with control, whereas basal cerebral blood flow of 20-week-old animals was not different from control. The results indicate a long-term role by the sympathetic nerves not only on vessel wall composition, but also on the regulatory capacity of the cerebral circulation.

Animals↗

PubMed1994

A morphometric study of the effect of bilateral cervical sympathetic ganglionectomy on the architecture of pial arteries in spontaneously hypertensive and normotensive rats.

The influence of the cranial sympathetic nerves on the architecture of pial arteries in normo- and hypertension was examined. For this purpose the effect of bilateral superior cervical ganglionectomy was evaluated in normotensive rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). The operations were performed at the age of 1 wk, which is just prior to the onset of ganglionic transmission. The length of the inner media contour was measured and the media cross-sectional area was determined planimetrically, with computerized digitalization of projected photographic images of transversely sectioned pial arteries. Four wk after sympathectomy there was a 20% reduction in media cross-sectional area and a consequent reduction in the ratio between media area and calculated luminal radius in the major pial arteries at the base of the brain in WKY but not in SHRSP. Conversely, in small pial arteries linear regression analysis showed that in WKY subjected to ganglionectomy the relationship between media cross-sectional area and luminal radius was significantly larger in arteries with a radius less than 21 microns compared to untreated WKY. No such effect was seen in the corresponding SHRSP vessels. In addition, the cross-sectional area of the internal elastic membrane (IEM) in the basilar arteries of WKY was measured by means of a computerized image-analysing system. Mean cross-sectional area of the IEM was approximately 45% larger following SE than in control animals. The present findings propose a 'trophic' role for the sympathetic perivascular nerves in large pial arteries of the rat. The increased media-radius ratio in the small pial arteries of the WKY following sympathectomy might reflect a compensatory hypertrophy due to reduced protection from the larger arteries against the pressure load. The inability to detect any morphometrically measurable effect of the sympathectomy in the cerebral arteries of SHRSP is probably explained by a marked growth-stimulating effect of the high pressure load in these animals.

Animals↗

PubMed1991

Lack of neural control and reactivity to vasoactive agents in malignant glioma arteries.

Vessels in malignant brain tumors have a defective blood-brain barrier. It is important to know if tumor vessels respond to vasoactive agents, since systemic administration of vasodilatory agents together with chemotherapy could increase the access of these drugs to the tumor. It was found that arteries in human malignant gliomas have no neural control and are totally nonreactive to various vasoactive agents. The vessels lose their reactivity within 1 to 2 mm outside the visible tumor front.

Brain Neoplasms↗

PubMed1990

Neuropeptide Y co-exists with vasoactive intestinal polypeptide and acetylcholine in parasympathetic cerebrovascular nerves originating in the sphenopalatine, otic, and internal carotid ganglia of the rat.

Neuropeptide Y co-exists with noradrenaline in the majority of the sympathetic nerves supplying cerebral blood vessels. However, after sympathectomy in the rat the number of cerebrovascular neuropeptide Y nerve fibers are only reduced in number despite a complete disappearance of the adrenergic markers. The origin of these non-sympathetic neuropeptide Y fibers was studied by nerve transections and retrograde axonal tracing utilizing True Blue. Three days after bilateral superior cervical sympathectomy, the number of neuropeptide Y-containing nerve fibers decreased to about 40% of that in non-treated animals. One week after True Blue application on the proximal portion of the middle cerebral artery, the tracer accumulated in neurons of the sphenopalatine, otic, and internal carotid ganglia. Of these cells 80%, 95% and 5%, respectively, were neuropeptide Y-positive. Some of the True Blue/neuropeptide Y-positive cells displayed immunoreactivity for vasoactive intestinal polypeptide and some were positive for choline acetyltransferase. Two weeks after bilateral removal of the sphenopalatine ganglion or transection of postganglionic fibers from the ganglion reaching the pial vessels through the ethmoidal foramen, together with subsequent sympathectomy, no neuropeptide Y-containing nerve fibers could be observed on the anterior cerebral and internal ethmoidal artery or the distal portion of the middle cerebral artery, whereas a few nerve fibers remained on the proximal portion of the middle cerebral artery, internal carotid artery, and the rostral portion of the basilar artery. In conclusion, neuropeptide Y in cerebrovascular nerves is co-stored not only with noradrenaline in sympathetic nerves from the superior cervical ganglion, but also with acetylcholine (reflected in the presence of choline acetyltransferase) and vasoactive intestinal polypeptide in parasympathetic nerves originating in the sphenopalatine, otic, and internal carotid ganglia.

Acetylcholine↗

PubMed1990

Amine-induced responses of pial and penetrating cerebral arteries: evidence for heterogeneous responses.

Middle cerebral arteries (MCAs) of rabbits were compared with two types of small branches (less than 100-microns outer diameter), penetrating arteries (PAs) and surface arteries (SAs), by determining their mechanical reactivity to several amines and standard contractile agents. Two techniques were employed: (a) measurement of isometric tension of 1-mm rings (MCA, PA, or SA); (b) measurement of perfusion pressure of segments consisting of essentially MCA or essentially PA. Both techniques revealed similar reactivity of the different types of vessel to acetylcholine, i.e., relaxations to a maximum of 52-78%, and similar strong contractile responses to histamine, although the MCA was more sensitive. Under H1 blockade, histamine dilated the PA (both techniques) and the MCA (perfusion technique), but not the SA. Relatively weak contractile responses to serotonin were observed in the MCA (both techniques) and the PA (perfusion technique), but not the SA (isometric tension only); no dilative responses could be elicited. Responses to noradrenaline varied with the vessel considered: The MCA contracted only, whereas the PA weakly contracted or relaxed at basal tone, and many preparations relaxed after precontraction with uridine triphosphate; the SA did not react. Relaxation of precontracted PA by noradrenaline occurred at relatively low concentrations and was antagonized by propranolol at 3 x 10(-7) or 3 x 10(-6) M. These results reveal very significant differences in the segmental reactivity to amines and suggest that noradrenaline released from sympathetic fibers might have opposing actions in the major pial arteries and the smaller penetrating branches.

Acetylcholine↗

PubMed1990

Selective electrical stimulation of postganglionic cerebrovascular parasympathetic nerve fibers originating from the sphenopalatine ganglion enhances cortical blood flow in the rat.

Recently, the origins and pathways of cerebrovascular acetylcholine- and vasoactive intestinal polypeptide-containing nerves have been elucidated in detail in the rat: The sphenopalatine ganglion is the major source for postganglionic parasympathetic fibers to the vascular beds of the cerebral hemispheres. To clarify the functional role of the nerves on cerebral blood vessels in vivo, brain cortical microvascular blood flow was measured in rats during electrical stimulation of these particular postganglionic fibers. Animals were subjected to transection of the right nasociliary nerve 2 weeks before the flow measurements to eliminate activation of peptidergic sensory fibers. Relative change in microvascular blood flow was continuously recorded by a laser-Doppler flowmeter system under alpha-chloralose anesthesia. The postganglionic fibers were electrically stimulated just proximal to the ethmoidal foramen by a bipolar platinum electrode (5 V; 0.5 ms; 3, 10, 30, 60 Hz; as a continuous stimulation for 90 s). Stimulation at 10 Hz induced a marked increase of the cortical blood flow (CoBF) on the ipsilateral side, whereas no change was observed on the contralateral side. It reached a maximum mean value of 42.5% at 46 s, and then slightly declined during the remaining stimulation period. No significant changes were observed in the mean arterial blood pressure or blood gases during or after stimulation. Both atropine and scopolamine failed to alter this flow increase. Electrical stimulation of the postganglionic fibers at different frequencies revealed a maximal increase in the CoBF at 30 Hz in the control situation (47.2%), but at 10 Hz after scopolamine administration (51.6%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Effect on cortical blood flow of electrical stimulation of trigeminal cerebrovascular nerve fibres in the rat.

It has recently been demonstrated in the rat that the majority of cerebrovascular pain fibres containing immunoreactive substance P and calcitonin gene-related peptide reach the vessels via the nasociliary nerve, a branch of the ophthalmic trigeminal division. In order to elucidate the effect of these nerves on blood flow in vivo, the relative changes in cortical microvascular flow were continuously monitored by a laser-Doppler flowmeter system during electrical nerve stimulation, with the central nerve connection cut and after removal of neighbouring dilatory parasympathetic nerves. The nasociliary nerve on one side was stimulated proximal to the ethmoidal foramen by a bipolar platinum electrode. Activation at different frequencies, continuously or as bursts with a constant voltage, impulse duration and total stimulus length, revealed that a maximum increase in blood flow amounting to 16.7% after 36 s was obtained with continuous stimulation at 10 Hz. Flow markedly declined during the following 1-min stimulation period. No changes in contralateral cortical blood flow, mean arterial blood pressure or blood gases were observed during or after stimulation. The present study demonstrates for the first time that direct and selective electrical activation of trigeminal cerebrovascular nerves induces an increase, albeit small and transient, in blood flow within the brain.

Animals↗

PubMed1989

Chronic nicotine treatment eliminates asymmetry in striatal glucose utilization following unilateral transection of the mesostriatal dopamine pathway in rats.

Partial hemitransection was performed through a knife lesion at the meso-diencephalic level in rats to sever the mesostriatal dopamine system. During the subsequent 2 weeks the animals received 0.125 mg/kg/h of nicotine continuously via an osmotic minipump implanted s.c. To achieve prompt high nicotine levels, 4 i.p. injections of 0.5 mg/kg nicotine were, in addition, given during the first 2 h following the lesion. The total treatment corresponded to a mean plasma level of 50 ng/ml nicotine, measured at the end of the experiment. Control animals received corresponding volumes of 0.9% saline. Quantitative autoradiographic analysis of the glucose utilization in the caudate nucleus using Sokoloff's [14C]2-deoxyglucose method demonstrated a 16% side-to-side difference in the lesioned control animals, whereas the asymmetry was counteracted by the nicotine treatment. Although there was an overall tendency to a lower rate of glucose utilization (by 6%) in the nicotine-treated animals compared to the controls receiving saline only, the difference was not statistically significant. The eliminated asymmetry probably reflects an increased survival of the dopamine neurons and/or of striatal nerve cells on the lesioned side due to protective effects of nicotine resulting from desensitization of nicotinic-type cholinergic receptors following continuous administration of the drug.

Animals↗

PubMed1989

Galanin-positive nerves of trigeminal origin innervate rat cerebral vessels.

(GAL)-positive nerve fibers in rat cerebral vessels were demonstrated by immunohistochemistry, and their origin in the trigeminal ganglia and pathway in the nasociliary nerve to the vessels was shown by retrograde tracer technique and nerve transection. Some fibres in the vertebrobasilar system appear to originate in extracranial sources. With the antiserum used only few GAL fibers could be seen in the vessels, mostly in the vertebrobasilar system. In neonatally sympathectomized animals a rich network could be visualized in most pial arteries - still particularly in the vertebrobasilar system - probably as a result of a diminished competition for nerve growth factor. No vasomotor effect of GAL could be detected in isolated segments of pial arteries, neither in normal nor in sympathectomized animals, which rules out a direct postsynaptic effect on vascular tone. GAL did not display prejunctional modulatory action on the adrenergic nerves present in the vascular preparations. A sensory function of GAL is discussed.

Adrenergic Fibers↗

PubMed1989

Studies of protective actions of nicotine on neuronal and vascular functions in the brain of rats: comparison between sympathetic noradrenergic and mesostriatal dopaminergic fiber systems, and the effect of a dopamine agonist.

Neuroprotective and possible trophic actions of nicotine were studied in two types of experimental models: (1) one in which the meso-striatal dopamine system was subjected to partial hemitransection, and regional glucose utilization (using 2-[3H]deoxyglucose) and blood flow (using [14C]iodoantipyrine) were measured by computer-assisted quantitative autoradiography based on a double-isotope technique; and (2) another where the sympathetic cranial nervous system supplying the brain vasculature was subjected to decentralization, axotomy, and partial or complete ganglionectomy, and the neuronal survival and fiber regeneration were elucidated by fluorescence histochemistry of noradrenaline, tyrosine hydroxylase, and neuropeptide Y. Continuous nicotine infusion for 4 weeks failed to significantly affect the neuronal response to the surgical interference of the sympathetic noradrenergic system. The same nicotine treatment for 2 weeks significantly improved glucose utilization and blood flow in caudate-putamen on the side in which the meso-striatal dopamine system had been transected, thus eliminating the 16% side-to-side asymmetry in the metabolism caused by the axotomy. The dopamine agonist, EMD 23,448, was without significant effect on this asymmetry. The hemitransection produced marked reduction in metabolism and flow also in the ventro-lateral thalamus. In substantia nigra, glucose utilization was markedly elevated--perhaps as a consequence of a regenerative increase in protein synthesis--opposite to a considerable reduction in nigral blood flow. Little or no effect of the hemitransection was seen in hippocampus or nucleus accumbens. In neither of these four regions did nicotine (or EMD 23,448) have any overt influence on glucose metabolism or blood flow. It is concluded that nicotine, mainly through its protective action on the meso-striatal dopaminergic system, is able to improve striatal glucose utilization and associated blood flow, probably reflecting a tendency to amelioration of neurotransmission function of surviving terminals belonging to the nigro-striatal dopamine neurons.

Animals↗

PubMed1989

Excitatory amino acids and cerebrovascular tone.

Levels of excitatory amino acids in the brain extracellular fluid compartment rise during pathological conditions in the brain such as ischaemia, anoxia and epilepsy. One such amino acid, glutamate, is present in sensory nerve fibres innervating, for example, cerebral vessels. Enhanced levels of circulating glutamate and aspartate are found in migraine sufferers. The present study examined whether excitatory amino acids, in concentrations found in the brain extracellular fluid compartment during pathological conditions, exert a direct effect on cerebrovascular tone. As tested in flow-regulating pial arteries from rat, cat and man, no such constrictive or dilatory effect was obtained.

Adult↗

PubMed1989

Characterization of dilatation induced by electrical field stimulation in mammalian cerebral and peripheral vessels.

The ability of electrical field stimulation in releasing transmitter from isolated blood vessels in vitro, during recordings of constrictor or dilator responses, is dependent upon an appropriate choice of stimulation parameters which avoid concomitant change in tone due to a direct effect on the vascular smooth muscle membrane. In many species, including man, small arteries such as pial arteries frequently respond to electrical field stimulation with a dilatation which is TTX-resistant. Such dilatations occur even with stimulus parameters of 7.5 V/60 mA at 0.1 ms, 6 Hz. The stimulation parameters required to induce the TTX-resistant response are just above those needed to obtain a purely neurogenic contractile or dilatory response in vessels equipped with a dense net of adrenergic nerves, such as rabbit central ear artery, and, in addition, highly sensitive postsynaptic alpha- or beta-adrenergic receptors, such as the buccal segment of the facial vein. This prompted us to characterize further the nature of the response. It was tested whether the relaxation, despite being TTX-resistant, might be neurogenic in origin. 4-Aminopyridine, in doses that usually enhance the transmitter release from nerves, did not affect the response. Blockade by a variety of dilator antagonists, the presence of excess amounts of known dilators or removal or emptying of known vasodilator nerves did not inhibit the response. Removal of extracellular calcium did not abolish the response. Therefore, it is highly unlikely that neuronal release is involved to any measurable extent in this response. The relaxation was not significantly affected by removal of endothelium, blockade of endothelium-derived relaxing factor, or interference with mast cells. At modest stimulatory parameters (12-13 V/96-104 mA at 0.1 ms, 7-8 V/56-64 mA at 0.3 ms, at 6 Hz) chlorine gas bubbles could be seen forming at the electrode or mounting hook; this gas is toxic to the musculature and relaxes a pre-contracted vessel. At stronger stimulation (greater than 12 V/96 mA, greater than 0.3 ms at 6 Hz) a relaxation supervened that was almost prevented by scavengers of oxygen free-radical metabolites. This relaxation was partly irreversible, indicating damage to the contractile elements. We conclude that when studying electrically induced release of vasodilator transmitters in vessels not equipped with an highly effective transmitter/receptor function, even a small rise in stimulatory parameters--in order to enhance transmitter release--causes relaxations that are non-neurogenic.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1989

Endothelin is a potent constrictor of human intracranial arteries and veins.

Endothelin, a peptide produced in endothelial cells, was found to be a potent constrictor of human pial arteries through a direct, slow action on the smooth muscle cell, with a pD2 value of 8.54. It was less potent as a constrictor in pial veins (pD2 7.80) and in branches of the middle meningeal artery and superficial temporal artery (pD2 7.61 and 7.77). The major component of the contractile response in the arteries comprises an effect on potential-operated calcium channels, as evidenced by tests with nimodipine. Endothelin may regulate intracranial vessels tonically during physiological as well as pathophysiological conditions.

Adult↗

PubMed1988

Vasoconstrictor effects in spinal cord of the substance P antagonist [D-Arg, D-Trp7,9 Leu11]-substance P (Spantide) and somatostatin and interaction with thyrotropin releasing hormone.

The present study was undertaken to investigate the possible effects of Spantide [D-Arg1, D-Trp7,9 Leu11]-substance P, a substance P antagonist, and of somatostatin on spinal cord blood flow. The experiments were performed with the laser-doppler technique on the L1 spinal cord segment exposed by laminectomy. The effect of Spantide was also studied in the rat with the [14C]iodoantipyrine technique. In addition, experiments were performed on rabbit skeletal muscle in vivo after administration of Spantide to the local vasculature. In the experiments on spinal cord, approximately the same doses were employed as those earlier shown to be "neurotoxic". When the vehicle alone (0.9% saline) was administered intrathecally, a slight decrease of brief duration was noted in the blood flow. Spantide, however, caused a dose-dependent decrease, where 2 micrograms caused an immediate drop of the blood flow to approx. 20% of its normal value. A total circulatory arrest was found in several animals. In most cases, the flow was gradually normalized, whereas the effect persisted for up to 60 min in others. Virtually the same effect was exerted by somatostatin. The experiments using the iodoantipyrine technique confirmed the effect of Spantide. Here, the high resolution of this method showed that the gray matter was affected preferentially, with a complete ischemic state or a drastically reduced flow in 4 out of 5 animals 10 min after 2 micrograms of Spantide; one animal was unaffected, and this animal did not show any signs of motor impairment. The vasoconstriction of Spantide was not affected by simultaneous injections with substance P. However, after i.v. pretreatment with thyrotropin-releasing hormone, at a dose that previously has been reported to be protective against the neurodegenerative effects of Spantide, blood flow was markedly increased as compared to Spantide alone. Results from the experiments using intravital microscopy flow studies in the rabbit tenuissimus muscle revealed that Spantide at the doses used had no vasoconstrictor effect in the skeletal muscle of this species. The results suggest that previous demonstrations of motor impairment and "neurotoxic" actions of intrathecally injected substance P antagonists and somatostatin may be related to a marked decrease in spinal cord blood flow. Counteraction of the effect of Spantide by thyrotropin-releasing hormone may be explained by its effect to increase blood flow.

Animals↗

PubMed1987

P1- and P2-purine receptors in brain circulation.

As there is increasing evidence that purines are involved in cerebral vasodilatation, purine receptors were characterized pharmacologically in pial arteries from rabbit, cat and man, and compared with purine receptors in various non-cerebral vascular beds. Use of agonists and antagonists allows purine receptors to be divided into P1 and P2 receptors. The location of these receptors on the surface of the various cells in the cerebrovascular wall was determined. P1 receptors, stimulated primarily by adenosine, are located on the smooth muscle cells, causing relaxation. P2 receptors, stimulated primarily by ADP and ATP, are located on endothelial cells and cause relaxation, and are also found on smooth muscle cells where they cause contraction. Slowly degradable ATP analogues were considerably more potent constrictors than ATP but not equally potent as dilators, which might indicate minor differences between the P2 receptors on smooth muscle and on endothelium. The P1 receptor was further subclassified into the A2 type. Adenosine may also reach an intracellular purine receptor, via an uptake process, to cause additional relaxation, as was shown with an intracellular purine receptor agonist in cat pial arteries. Brain vessels were found to be considerably more sensitive to purines than most non-cerebral vessels studied.

2-Chloroadenosine↗

PubMed1987

Blood-brain barrier leakage and brain edema in stroke-prone spontaneously hypertensive rats. Effect of chronic sympathectomy and low protein/high salt diet.

Brain edema associated with severe chronic hypertension was studied in stroke-prone spontaneously hypertensive rats (SHRSP), 5 to 9 months of age. Blood-brain barrier (BBB) leakage sites and intracerebral spreading pathways for plasma proteins were delineated by an intravenously (i.v.) injected exogenous dye tracer (Evans blue), known to form a complex with albumin in blood, and by immunohistochemical visualization of extravasated endogenous plasma proteins. The tissue content of edema fluid was estimated by measuring the specific gravity of selected brain regions, stained or unstained by the tracer dye, on a bromobenzene-kerosene gradient column. Multifocal BBB leakage sites were macroscopically detected within the cerebral cortex and the deep gray matter after i.v. circulation of Evans blue-albumin for 30 min. After 24 h of i.v. circulation the dye tracer had spread not only locally in the gray matter but also into the adjacent white matter, where it was widely distributed. Immunohistochemically visualized plasma proteins showed similar distribution. Unilateral superior cervical ganglionectomy performed at 4 weeks of age neither increased the incidence of major BBB opening to Evans blue-albumin nor altered the specific gravity of the ipsilateral cerebral hemisphere in grown-up SHRSP, furthermore, the blood pressure remained unchanged. The lack of significant effect on BBB function may possibly be attributed to the extensive reinnervation of the cerebral arteries, verified in the grown-up SHRSP using the Falck-Hillarp fluorescence method for visualization of catecholaminergic nerve fibers. In SHRSP raised on a low-protein and high-salt diet the mean arterial blood pressure was 212 mm Hg compared to 195 mm Hg in controls (P less than 0.05) and the incidence of BBB opening was 72% compared to 25% in controls (P less than 0.05). After 24 h of i.v. circulation of Evans blue-albumin, brain regions stained by the dye tracer showed significantly reduced specific gravity (P less than 0.001), while unstained regions had normal values. Thus the brain edema fluid spread, as revealed by specific gravity measurements, corresponded to the intracerebral distribution of extravasated plasma proteins.

Animals↗

PubMed1987

Vasomotor effects of neurotransmitters and modulators on isolated human pial veins.

Vasomotor reactivity of human pial veins, obtained in conjunction with neurosurgical operations, was studied in vitro. The effect of transmitters in nerves previously recognized in these vessels, as well as that of neuromodulators, was characterized. A comparison of these effects with their effects in the nearby pial arteries of the same patients was made. It was found that the veins were equipped with more sensitive alpha-adrenergic receptors (lower EC50 values) than the arteries. The reverse was found for 5-hydroxytryptamine. Acetylcholine, which causes an endothelium-dependent dilation of pial arteries, contracted the veins despite an apparently intact endothelium. Considering the lower maximum values in veins, responses to histamine, the neuropeptides calcitonin gene-related peptide, bradykinin, and neuropeptide Y; and prostaglandins (PGE1 and PGF2 alpha) were principally the same in the arteries and veins. The dilatory responses to vasoactive intestinal polypeptide and substance P were less pronounced in veins than in arteries. The veins only transiently contracted to a depolarizing potassium solution; calcium influx promotors and inhibitors, as well as calcium-free solution, did not affect the contractile ability of the vein, contrasting to the reactivity of the artery. This clearly indicates that the veins are not substantially dependent upon calcium influx for their acute contractile ability.

Cerebral Veins↗